Regulation of liver carnitine palmitoyltransferase I gene expression by hormones and fatty acids

Author:

Louet J.-F.1,Le May C.1,Pégorier J.-P.1,Decaux J.-F.1,Girard J.1

Affiliation:

1. Centre de Recherche sur I'Endocrinologie Moléculaire et le Développement, UPR 1524 CNRS, 9 rue Jules Hetzel, 92190 Meudon, France

Abstract

This brief review focuses on the transcriptional regulation of liver carnitine palmitoyltransferase I (L-CPT I) by pancreatic and thyroid hormones and by long-chain fatty acids (LCFA). Both glucagon and 3,3′,5-tri-iodothyronine (T3) enhanced the transcription of the gene encoding L-CPT I, whereas insulin had the opposite effect. Interestingly, the transcriptional effect of T3 required, in addition to the thyroid-responsive element, the co-operation of a sequence located in the first intron of L-CPT I gene. Non-esterified fatty acids rather than acyl-CoA ester or intramitochondrial metabolite were responsible for the transcriptional effect on the gene encoding LCPT I. It was shown that LCFA and peroxisome proliferators stimulated L-CPT I gene transcription by distinct mechanisms. Peroxisome proliferator stimulated L-CPT I gene transcription through a peroxisome-proliferator-responsive element (PPRE) located at -2846 bp, whereas LCFA induced L-CPT I gene transcription through a peroxisome-proliferator-activated receptor α (PPARα)-independent mechanism owing to a sequence located in the first intron of the gene.

Publisher

Portland Press Ltd.

Subject

Biochemistry

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